Activation of protein kinase C augments peptide release from rat sensory neurons

Lisa A. Barber, Michael R. Vasko

Research output: Contribution to journalArticle

83 Scopus citations


To determine whether protein kinase C (PKC) mediates release of peptides from sensory neurons, we examined the effects of altering PKC activity on resting and evoked release of substance P (SP) and calcitonin gene-related peptide (CGRP). Exposing rat sensory neurons in culture to 10 or 50 nM phorbol 12,13-dibutyrate (PDBu) significantly increased SP and CGRP release at least 10-fold above resting levels, whereas the inactive 4α-PDBu analogue at 100 nM had no effect on release. Furthermore, 100 nM bradykinin increased peptide release approximately fivefold. Down-regulation of PKC significantly attenuated the release of peptides evoked by either PDBu or bradykinin. PDBu at 1 nM or 1-oleoyl-2-acetyl-sn-glycerol at 50 μM did not alter resting release of peptides, but augmented potassium- and capsaicin-stimulated release of both SP and CGRP approximately twofold. This sensitizing action of PKC activators on peptide release was significantly reduced by PKC down- regulation or by pretreating cultures with 10 nM staurosporine. These results establish that activation of PKC is important in the regulation of peptide release from sensory neurons. The PKC-induced enhancement of peptide release may be a mechanism underlying the neuronal sensitization that produces hyperalgesia.

Original languageEnglish (US)
Pages (from-to)72-80
Number of pages9
JournalJournal of Neurochemistry
Issue number1
StatePublished - Jul 1996


  • Calcitonin gene-related peptide
  • Phorbol esters
  • Protein kinase C
  • Sensory neurons
  • Substance P
  • Transmitter release

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

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